Related Experiment Video
Updated: Jul 6, 2025

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
Published on: June 23, 2013
PRMT2 silencing regulates macrophage polarization through activation of STAT1 or inhibition of STAT6
Ting Liu1, Yinjiao Li1, Muqiu Xu1
1Department of Anesthesiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Background:
Macrophages play significant roles in innate immune responses and are heterogeneous cells that can be polarized into M1 or M2 phenotypes. PRMT2 is one of the type I protein arginine methyltransferases involved in inflammation. However, the role of PRMT2 in M1/M2 macrophage polarization remains unclear. Our study revealed the effect and mechanism of PRMT2 in macrophage polarization.
Methods:
Bone marrow-derived macrophages (BMDMs) were polarized to M1 or M2 state by LPS plus murine recombinant interferon-γ (IFN-γ) or interleukin-4 (IL-4). Quantitative polymerase chain reaction (qPCR), western blot and flow cytometry (FCM) assay were performed and analyzed markers and signaling pathways of macrophage polarization.
Results:
We found that PRMT2 was obviously upregulated in LPS/IFN-γ-induced M1 macrophages, but it was little changed in IL-4-induced M2 macrophages. Furthermore, PRMT2 konckdown increased the expression of M1 macrophages markers through activation of STAT1 and decreased the expression of M2 macrophages markers through inhibition of STAT6.
Conclusions:
PRMT2 silencing modulates macrophage polarization by activating STAT1 to promote M1 and inhibiting STAT6 to attenuate the M2 state.
Insights
Protein arginine methyltransferase 2 (PRMT2) influences macrophage polarization. Silencing PRMT2 promotes M1 macrophage markers via STAT1 activation and reduces M2 markers by inhibiting STAT6.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Macrophages are key innate immune cells, exhibiting M1 (pro-inflammatory) and M2 (anti-inflammatory) polarization.
- Protein arginine methyltransferase 2 (PRMT2) is implicated in inflammatory processes.
- The specific role of PRMT2 in M1/M2 macrophage polarization remains largely uncharacterized.
Purpose of the Study:
- To investigate the effect of PRMT2 on macrophage polarization.
- To elucidate the underlying molecular mechanisms by which PRMT2 influences M1/M2 macrophage phenotypes.
Main Methods:
- Bone marrow-derived macrophages (BMDMs) were differentiated and polarized into M1 or M2 states.
- Stimuli included lipopolysaccharide (LPS) with interferon-gamma (IFN-γ) for M1, and interleukin-4 (IL-4) for M2 polarization.
- Techniques employed were quantitative polymerase chain reaction (qPCR), western blot, and flow cytometry (FCM) to assess markers and signaling pathways.
Main Results:
- PRMT2 expression was significantly upregulated in M1 macrophages induced by LPS/IFN-γ, with minimal change in M2 macrophages induced by IL-4.
- Knockdown of PRMT2 enhanced M1 macrophage markers, correlating with STAT1 activation.
- PRMT2 knockdown also decreased M2 macrophage markers, associated with STAT6 inhibition.
Conclusions:
- PRMT2 plays a crucial role in modulating macrophage polarization.
- PRMT2 silencing promotes M1 polarization by activating STAT1.
- PRMT2 inhibition of STAT6 contributes to the attenuation of the M2 macrophage state.
Related Concept Videos
The JAK-STAT Signaling Pathway
PI3K/mTOR/AKT Signaling Pathway

